Merged Consortia Forge Path to Trials in Frontotemporal Dementia FTD Fluid Markers for Degeneration: Check. For Pathology: Not Yet. Imaging Exposes Hugely Heterogeneous Brain Changes Among FTDs Moving Target: Can Standardized Tests Track Symptoms of FTD?
Donanemab Confirms: Clearing Plaques Slows Decline—By a Bit Astroglial Markers Poised for Stardom? Shuttle Unloads More Gantenerumab Into the Brain N-Terminal Tau Antibodies Fade, Mid-Domain Ones Push to the Fore Where to Now, Phospho-Tau? Clinicians from
The first ultrasensitive plasma test for this old marker differentiates Alzheimer’s from healthy controls and non-AD dementias. It segregates people stepwise at phases of pathogenesis down to Braak stages 1 and 2 and below amyloid PET positivity.
In mice, an anti-ApoE antibody removed plaques from the brain’s parenchyma and blood vessels better than aducanumab. Importantly, it caused no microhemorrhages.
The commercial test uses a few drops of saliva. It must be ordered by a physician. Plans are also in the works to use the test to select participants for clinical trials.
Based on pooled data from five well-characterized cohorts, women appear to initially outperform men, but then slide faster, on global cognition and executive function. Oddly, this was not true for memory.
White matter-associated microglia express similar genes to plaque-associated DAMs. They seem to be triggered by the myelin breakdown associated with aging and disease.
Grappling with a rare disease whose variability is daunting, international cohort studies are charting the natural history of FTD. They have discovered biomarkers and honed physiological tests that underlie its behavioral symptoms.
The global platform trial for Alzheimer’s due to mutations in APP or presenilin will try to treat or prevent symptoms by deploying a therapeutic antibody that homes in on a piece of tau known to aggregate into neurofibrillary tangles.